​Dr. Kiki Chang, is a child psychiatrist with over 22 years of experience in working with younger children, adolescents, adults and families. Formerly, Dr. Chang was Professor of Psychiatry and Behavioral Sciences at Stanford University School of Medicine and co-founder of the Stanford PANS Clinic. His specialty is working with youth and young adults who have or are at risk for serious mood disorders, such as depression or bipolar disorder as well as PANS/PANDAS and related neuropsychiatric disorders. Dr. Chang will be presenting a webinar August 27, 2019 for Continuing Medical Education Credit.

Thank you to Dr. Chang for allowing Foundation For Children With Neuroimmune Disorders president and founder, Anna Conkey to interview him.

How did you first learn of PANS/PANDAS and what motivated you to begin treating children with PANS/PANDAS?

I first became interested when I realized that some patients who were referred to me for consultation with presumed bipolar disorder had an unusual onset and/or course. These patients were also treatment resistant to standard treatments for bipolar disorder. I discovered that many of them either met PANS criteria or had a periodic mood disorder that included elements of catatonia, or unusual mental status changes. It made sense that underlying immunologic factors were at least partially responsible. These patients responded to immunomodulatory treatments rather than typical psychotropics.

I also started collaborating with a pediatric rheumatologist, Dr Jennifer Frankovich, who was interested in the same patients from the other end – many of her patients with rheumatologic disorders also had psychiatric symptoms including OCD. When we realized our shared interests and that these patients fell under the PANS rubric, we decided to join forces with Margo Thienemann and start the PANS Clinic at Stanford.

Do you ever treat children who did not have an abrupt or acute onset, and if so, do they respond similarly to children who did have an abrupt onset?

Yes I do, and not always. Abrupt is an arbitrary but necessary concept – is it 48 hours? 72 hours? In our 2013 Expert Consensus Diagnostic meeting we agreed on 72 hours but many kids with sub-acute onset, say one week, will still likely have the same underlying issues – it’s just that if you keep stretching out that onset time, then it becomes a gray area and muddies the research waters. The longer and more gradual the onset, the less likely it will fit clear PANS criteria and also have the same treatment response.

How do you determine which patients with PANS would benefits from psychiatric medications and when to introduce them?

I think our guidelines present this issue fairly well (first author Dr Margo Thienemann, JCAP 2017). If needed, psychiatric support is always indicated – to help alleviate severe anxiety, agitation, sleeplessness, etc. If patients are functioning OK without them, then I prefer to treat medically as long as possible before using psychotropics. At some point, whether due to only partial treatment response medically, or other factors, psychotropics make a lot of sense.

Is there a particular class of psychotropic medication that tends to be more effective in children with PANS?

I have a particular fondness for lithium, in that for youth with severe mood disruption, including a bipolar like picture, even in a PANS context, it can be very useful. Yes, lithium has potential side effects, but if it works, it works great. I could go on and on about the benefits of lithium and how it is missing in our soil, water, and diets, but you probably have a word limit.

Are there any anomalies you see when treating children with PANS with psychotropic medications?

Not sure what you mean – do you mean do SSRI’s sometimes worsen their course? Sure, but not always. Also antipsychotics sometimes cause EPS symptoms more so than would be expected. Probably due to the dopamine dysregulation going on in the basal ganglia being compounded by a dopamine receptor antagonist.

Many medical providers have interpreted the JCAP treatment guidelines as step one, “Psychiatric and Behavioral Interventions,” step two, “Use of Immunomodulatory Therapies,” and step three, “Treatment and Prevention of Infections.” As one of the authors, was the intent to suggest psychiatric and behavioral interventions prior to other interventions or has this been misinterpreted?

Yes, that would be a misinterpretation of the treatment guideline! It’s really based on the patient’s presenting issues. All three approaches should be considered initially. The order depends on what’s going on with the individual patient. If there is clear infection, then of course treat it first. If psychiatric symptoms are severe and need urgent stabilization, then do that. I had no idea people were interpreting the guidelines that way, I think the introduction paper to the guidelines explains the overall approach well.

Have you treated any patients with longstanding diagnoses of bipolar, schizophrenia, depression, or any mood disorders whose symptoms resolved with immunomodulatory therapies?

Yes, on occasion. I saw the recent report from Japan about the patient with schizophrenia whose symptoms resolved with bone marrow transplantation after a subsequently diagnosed cancer. Absolutely make sense in SOME cases. Great example – clozapine has a long history of working where other antispychotics have failed – for schizophrenia or bipolar disorder. Why? The receptor profile is similar to other atypical antipsychotics – so what sets it apart? Well, the one main side effect people have to check for is agranulocytosis, or basically suppressing the body’s production of white blood cells. Hmm…so a potential “side effect” is suppressing the immune system? Seems like not a coincidence to me – it probably affects the immune system in some way even when not having full suppression of neutrophil production…and that is in my opinion probably why it works when other medications don’t…that perhaps those patients have a more immune-mediated illness.

What is your approach to managing children with autism who develop neuropsychiatric symptoms? How does this differ from your approach to those without autism?

Tough question. Certainly just because you are diagnosed with an autism spectrum disorder doesn’t mean you CAN’T develop a PANS condition. Some might argue that these kids might be actually MORE susceptible to such a condition, given the propensity of kids with ASD to have OC symptoms and/or tics. My approach does not differ really for treatment, but for diagnosis there must be a clear acute onset meeting PANS criteria in order to say, yes this is PANS and let’s treat accordingly.

If you could snap your fingers and have any research on PANS completed tomorrow, what would you most like to see studied?

Egads, great question, there are so many studies I would like to see done. I’d have to say probably first to have placebo controlled steroid trials in youth with PANS. Clearly clinically steroids can be effective, but it would help tremendously to have this proven in a RDBCT. Oh and having a cleaner and longer IVIG trial completed – and if positive then getting an indication so that insurance companies will all have to cover it for these kids.

Autism Spectrum Disorder (ASD) The Question Every Parent should ask.… Why is This Not Medical?

October 26, 2018

Michael Goldberg, MD

There are different kinds of childhood disorders, yet none scientifically or medically can remotely affect the CDC reported 1:36 children and be thought of as genetic or developmental in origin, unless, medical science is ignored and that child is NOW labeled, ASD Autistic! However, given the horrific and increasing numbers of ASD affected children, there must be an underlying unidentified medical disease presenting with autistic like symptoms and behaviors i.e. an ASD “PHENOTYPE”!

It is scientifically impossible to have an epidemic without a disease origin. Mistakenly labeling and then treating children as “psychiatric Autistic” is the failure of our medical system to recognize these children are really part of an enlarging, unrecognized medical pandemic affecting children and young adults. ASD (1:36) today is worse than the Polio epidemic (1:1500 – 1:2000) of the 1950’s.

As early as the 1960s, certainly in the 1970s, pediatricians were being taught at UCLA and other excellent medical schools that Psychiatric, DSM autism affected 1 – 2 in 10,000 children. Further, those 1-2 children, in order to be labeled Autistic must never be affectionate/ never normal! To have that number mysteriously begin to increase in the 1990s to the astounding level of 1 in 36 otherwise affectionate children begs the questions; “Is this epidemic? And if so “Why is this condition not considered and treated as medical?”

Instead of being excited about the arrival of new baby, watching a child grow and prosper, sadly many mother’s today (expressed constantly when meeting new parents) live with perhaps worse fears than parents and families of the 40s and 50s. At that time the polio epidemic was a real threat, affecting 1:1500 – 1:2000 children, and the world mobilized to find a cure. Today ASD affects 1:36 and climbing! Where is the medical community? You cannot have an epidemic of psychiatric or developmental conditions!

I am proposing an answer to the question, nobody in public health, academic research or the pediatric medical community dare to acknowledge or ask: Is ASD in children and young adults a medical condition? Are they medically ill and thus treatable?

My answer: YES and the medically treatable symptoms and manifestations are directly related to Herpes viruses (potentially others) and the immune system!

Medical School of the 1970s was eventful. Professors opined we were entering a “golden age” of medicine, because “common” pathogens were being identified and eradicated. As new physicians we recognized we live in a sea of viruses. We were protected by our immune system and its adaption over thousands of years.

Nobel level professors taught there were differences between “normal” viral titers (markers) and “elevated” viral titers, indicating the presence of an active virus. Then in the early – mid 1980s very powerful medical leaders (CDC, NIH) unexplainably decided elevated Herpes viral titers in children and adults were meaningless! Lab evaluations of “normal” vs. elevated, are still carried over today, but “ignored” when elevated. As a practicing pediatrician, to suddenly be required to ignore the role of the Herpes virus was and still is beyond comprehension.

The Medical Literature still support the significance of a fourfold change in viral titers. However, if a pediatrician does not consider or is precluded from testing for viral titers, how can the physician begin to evaluate or “rule out” if there is treatable viral activity? She/he cannot! How does that benefit the child or the family? It does not! For a physician to leave a child with overwhelming sensory issues, without a complete medical work up is unconscionable. In my opinion, to discount and ignore elevated viral titers in children and young adults remains one of the biggest travesties being perpetrated upon our children by the current medical system.

All of the ASD labeled children I am working up are affectionate. Many present with this ASD “phenotype”. Typically, their blood tests show elevated viral titers for the HHV6 herpes virus, Epstein Barr and/or CMV virus. In addition, many of these children also present with outright early developmental delays and motor issues. For these issues, I was taught by excellent professors to think of viruses, “rule-out viruses.”

Most children having issues today become labeled as “on the ASD spectrum” without a proper medical workup and investigation for illness, chronic viral activation issues, etc. By artificially removing the medical criteria developed over decades past, the current “system” too quickly, attaches the label of ASD. The pediatrician unwittingly abandons the children and parents to the psychiatric community for behavior training and a life of isolation and despair. Parents are told to cope and forego their focus or desire to pursue real medical answers and real potential help for their children. How much worse can this get before parents and others step up and declare “enough is enough”!

In my professional opinion based upon over 40+ years of clinical experience, “Autism spectrum disorder” (not meeting strict Kanner criteria) with accompanying language impairment is in reality a medical disease (complex immune – complex viral) presenting as an encephalopathy (often viral) with “autistic” symptoms.

The language impairment in these ASD labeled children is part of the disease, not secondary to Autism Spectrum Disorder. Many of my patients (approx. 75+%) respond favorably to a medical protocol of anti-viral medications and diet modifications, eliminating known allergenic foods. This anti-viral component mitigates the effects of the viruses to the brain, while the diet changes reduce stress on the body, the brain, and the immune system. Additional improvement is achieved with the use of an SSRI (Selective Serotonin Reuptake Inhibitor). The SSRI is introduced not for “depression,” but as a pharmaceutical/medical way to treat temporal lobe hypo perfusion; a real, medically definable, physiologic CNS dysfunction evidenced on a NeuroSPECT scan

This medical protocol results in the elimination or severe abatement of the “autistic” like symptoms and behaviors and allows an increase in, a return of, higher cognitive function. The most common phrase I hear from parents of improving children is,

“It is as if a fog has lifted.”

and from speech and other therapists,

“This is not the same child I have been working with.”

These otherwise affectionate “typical/normal” (now much brighter cognitively) children are now placed in a position to be taught (not trained), allowed to “catch up” and progress with their peers. For whatever reasons, those in positions of authority refuse to acknowledge or investigate this treatable complex immune, complex viral medical problem. Instead, current focus and research is on “causation” with activated “gene expressions” or “complex genetic” ideas being proffered as the origin.The reality is a treatable underlying viral/immune process is being ignored! The “system” has become so biased, against the obvious, that good professors wishing to pursue research into a readily treatable complex immune, complex viral causation, have not only been refused funding, but fear losing their positions. These short-sighted money decisions at the clinical level mean the loss of the near immediate relief from ASD behaviors and mannerisms, improved, often excellent cognitive abilities, and improvement in the future quality of life for the child and family. Why?

Recently I met with a group of educators discussing the “differences” working with a medically treated ASD child (stressing an ASD “phenotype,” not developmental “autism”). They were aware the medically treated child was able to understand and be taught! These educators realized this was an emerging potentially regular child, not a child mysteriously born “miss-wired.” Thankfully, there are excellent academic professors who also know something is seriously wrong, literally acknowledging we are in a missed medical “pandemic”.

An appropriately focused and engaged medical community together with key medical and academic researchers, could create a pathway for a healthier future for the children and reduce the financial costs to all affected, including our social and educational systems.

The Duke study is remarkable in that 60-70% or more of children with Autism have de novo gene mutations (not found in either parent) that must have occurred after birth according to the results, not in the egg, sperm or early utero development as previously, and erroneously assumed.This new finding reveals research should now be geared to finding out what environmental damage after birth leads to these mutations and/or what pathogens are acting as triggers.Autism like Lyme/MSIDS is a pandemic and according to one Wisconsin LLMD, 80% of his Autistic patients are also infected with Lyme/MSIDS.

Boy’s Lyme Disease Morphs into Autoimmune encephalopathy. It took 10 years and 20 doctors to find out 12-year-old Patrik had Lyme disease. Just 4 months later the doctors discovered he also has a condition where his immune system attacks his brain. Dr. Souhel Najjar, Cahalan’s doctor, heroically saves the day again.

MacDonald states that both worms and borrelia can cause devastating brain damage and that,

“while patients are wrongly declared free of Lyme and other tick-borne infections, in reality, too often they contract serious neurodegenerative diseases which can kill them.”

MacDonald made his discovery from 10 specimens from the Rocky Mountain Multiple Sclerosis Center Tissue Bank. All 10 showed evidence of borrelia infected nematodes. Five patients who died of Glioblastoma multiforme, a malignant brain tumor, and four patients who died of Lewy Body dementia also showed infected nematodes.MacDonald used FISH, Fluorescent In Situ Hybridization, which uses molecular beacon DNA probes to identify pieces of borrelia’s genetic material which fluoresce under the microscope with a 100% DNA match.

Physicians need to take this disease seriously.

According to Margo Thienemann, MD, clinical professor of psychiatry and behavioral sciences at Stanford, and the lead author of the portion of the guidelines that address psychiatric and behavioral interventions, treatment is at least tri-part:

Toxic metal pollution linked with development of autism spectrum disorder

Russian researchers, together with their foreign colleagues, have demonstrated that environmental metal and metalloid pollution (lead, mercury, aluminum, and arsenic) may induce autism spectrum disorders (ASDs), and have considered possible mechanisms of exposure to these substances. The study may be useful for the prevention and therapy of ASD. The article is published in the journal Environmental Research.

Autism spectrum disorder is a group of disruptive neurodevelopmental disorders that cause problems in communication, socialization, and limited interests. They appear usually at the age of three years. Over the past 20 years, the prevalence of ASD has increased by 30 percent globally, although scientists have not yet reached a consensus on the causes and mechanisms of the disorder. Genetic mutations correspond to approximately 7 percent of cases of ASD. Such mutations can occur under the influence oftoxic metals in the first months of prenatal and postnatal life, when the nervous system is especially sensitive to toxic environmental pollutants. This hypothesis is confirmed by recent studies. For example, scientists from RUDN University with their colleagues from Saudi Arabia and Norway have observed increased lead and mercury levels in association with selenium deficiency in erythrocytes of children with ASD. A large Korean study including 458 mother-child pairs showed a clear link between exposure to mercury in early childhood and autistic behavior at the age of five.

But how, exactly, can toxic metals cause ASD? Researchers of the RUDN University and Yaroslavl State University, under the guidance of Prof. Anatoly Skalny, believe that the main mechanism underlying the onset of ASD is inflammation in brain nervous tissue. The latter is related to increased levels of pro-inflammatory cytokines—signaling peptide molecules. In addition, arsenic disrupts the metabolism of neurotransmitters and promotes epigenetic changes. Finally, aluminum can cause dysfunction of glia – non-neuronal auxiliary cells of the nervous tissue, which play an important role in the functioning of the nervous system. These assumptions are confirmed by the results of the authors’ studies, which demonstrated a tight association of the level of toxic elements in the blood serum of children with ADS and neuroinflammatory markers.

Researchers from the RUDN University considered the link between exposure to three toxic metals (lead, mercury, aluminum) and arsenic with the emergence of ASD in children. They proposed three main processes that occur under the influence of toxic metals and contribute to the development of autism: neuroiflammation, apoptosis (programmed cell death), and excitotoxicity. In addition, the scientists proposed preventive measures and approaches that reduce the risk of ASD.

“Unfortunately, the contemporary methods of metal detoxification do not allow to achieve ASD remission, especially since their effectiveness in ASD is not confirmed from the positions of evidence-based medicine,” noted the co-author of the article Alexey A. Tinkov, M.D., Ph.D., senior lecturer of the Department of Medical Elementology of the RUDN University.

In the case of acute intoxication, the use chelating agents (DMPS, DMSA, CaEDTA and BAL) is recommended, but in the case of ASD, chronic metal overload usually takes place. Moreover, chelators also have a significant number of side effects. In the case of chronic intoxication, toxic metals can be successfully eliminated from the body by functional foods. A number of phytochemicals (polyphenols, etc.) decrease lead toxicity. In turn, laboratory data demonstrate that zinc and selenium compounds significantly reduce toxicity of lead, arsenic and cadmium.

Researchers recommend the use of a comprehensive approach for the correction of metal overload in ADSs. Particularly, in addition to elimination of metals exposure, it is proposed to use antioxidants and anti-inflammatory compounds, as well as supplements containing heavy metal antagonists (selenium, zinc), and adhere to a diet.

Dr. Richard Frye is a pediatric neurologist and Chief of The Division of Neurodevelopmental Disorders at Phoenix Children’s Hospital. He’s recognized as an expert on the treatment of autism.

Could you summarize the results of your recent study, “Intravenous Immunoglobulin For The Treatment Of Autoimmune Encephalopathy In Children With Autism”?

Our study recently published in Translational Psychiatry showed that a subset of children with autism spectrum disorder (ASD) who did not respond to standard interventions had autoantibodies in their blood targeting brain tissue which might qualify them for the diagnosis of autoimmune encephalopathy (AIE). The majority of children with ASD had elevated levels of autoantibodies measured by the Cunningham Panel™ (Moleculera Labs, Oklahoma City, OK) along with an elevation in the activation of calcium calmodulin dependent protein kinase II (CaMKII). A few patients had other brain targeted autoantibodies associated with AIE, such as voltage-gated calcium channels autoantibodies.

Some of the patient qualifying for the diagnosis of AIE were treated with intravenous immunoglobulin (IVIG) and their symptoms were monitored with two widely-used validated behavioral questionnaires, the Aberrant Behavior Checklist (ABC) and the Social Responsiveness Scale (SRS). Overall, IVIG was found to improve scores on both the ABC and SRS questionnaires and the great majority of parents reported improvements in additional symptoms related to ASD. The majority of patients experienced side effects from the IVIG treatment but most of the time these were mild and limited to the time around the infusion period. We were also able to divide the patients who received IVIG into those that demonstrate a positive response on the behavioral questionnaires and those that did not. This allowed us to determine if autoantibody titers of the Cunningham Panel™ collected prior to IVIG treatment could predict which individuals would response to IVIG. We found that, overall, the Cunningham Panel™ could predict which individuals would response to IVIG treatment with over an 80% accuracy rate and that the anti-dopamine receptor D2L and anti-tubulin antibodies were particularly sensitive to predicting response to IVIG treatment.

What initially led to your interest in considering immune-mediated factors in autism?

I have built my clinical practice with a vision of discovering new treatments for children with ASD. Some children with ASD do not respond to standard treatments or even new novel treatments and many times a standard medical workup does not reveal any additional obvious treatment targets. Such patients need to be investigated further to determine if there are other factors preventing them from developing skills or causing disruptive behaviors. For me, integrating an investigation of immune factors into my practice was the next step for further determining treatable factors for children with autism.

Do you have a sense for the percentage of children with autism who also have AIE?

The study describes 82 patients that were screened for AIE. This was about 8% of the patients seen in my autism clinic during the study period. 60% of these children were believed to probably have AIE, or about 5% of the children seen in my autism clinic. The percentage of the other 92% of patients seen in my autism clinic that might also have AIE is not known but it is very likely that a significant percentage of these children may have AIE. Many of these children were not investigated further because of various reasons including insurance coverage of testing, parental preference and/or difficultly in drawing blood. Further studies that systematically evaluate the general ASD population for AIE so we have a better understanding of the number of children with ASD that may benefit from treatment for AIE.

While acceptance of post-infectious autoimmune encephalopathy and pediatric acute-onset neuropsychiatric syndrome (PANS) continues to grow, there seems to be a bias within the medical community against considering PANS in children with autism. Would you agree or disagree with this statement and do you have a sense for why this might be?

I believe that the idea that there are physiological abnormalities underling ASD which can be treated is novel concept that is faced by significant skepticism. Also many are skeptical that children with ASD can recover from their disorder at all. This skepticism, I believe, it based on an old concept of children with neurodevelopmental disorders having a “static encephalopathy” in which it is believed the brain is damaged and cannot improve. As new research connects neurodevelopmental and neurobehavioral disorders such as ASD with abnormal physiology and treatments that target these physiological abnormalities, evidence will become more compelling. As treatments are shown to improve function in disorders which previously had few effective treatments, I believe more people in the medical community will embrace treatments that help children with neurodevelopmental disorders.

Some physicians have questioned the validity of the Cunningham Panel due to the fact that many children with autism have positive results. The conclusion by some is that this means the test is producing false positive results. How would you respond to this?

In our study 57% of the children we tested were positive for the Cunningham panel as we defined a positive test. We set a more stringent criteria as compared to others. For our clinical practice, the Cunningham panel is considered positive when one or more autoantibodies are elevated AND CaMKII is elevated. One of the reasons we examined the predictability of the Cunningham panel is to validate and refine the accuracy of the Cunningham panel. Our study points to two particular autoantibodies which appear to predict response. Since the components of the Cunningham panel have been developed based on converging animal and human basic research, it is very clear that these components are very likely to be very meaningful. It is likely that different components (or combination of components) will identify different subgroups of neurobehavioral, neuropsychiatric and/or neurodevelopmental disorders. Further studies are needed to further refine the most accurate use of interpreting the components of the Cunningham panel.

Do you ever treat children who did not have an abrupt or acute onset of neuropsychiatric symptoms, and if so, do they respond similarly to children who did have an abrupt onset?

Abrupt onset of neurological, behavioral or psychiatric systems as well as abrupt loss of previously acquired skills are red flags for an underlying metabolic or immunological disorder. All three cases described in our recent paper had abrupt onset of symptoms and approximately one-third of children with ASD are estimated to have neurodevelopmental regression. However, there are children without a history of an abrupt onset of systems who also respond to immune and metabolic treatments that target medical abnormalities usually associated with an acute onset of disease. Thus, I do not usually use the history of abrupt symptoms onset to guide my workup. Treatments I prescribed are guided by biomarkers.

What is your approach to managing children with autism who develop neuropsychiatric symptoms? How does this differ from your approach to those without autism?

I have found that many children with neuropsychiatric symptoms without ASD have similar metabolic and immune abnormalities as those with ASD. I use the same approach for such children and have had successes in improving their symptoms and ability to function.

Is there any research you’re working on currently that you’d be willing to tell us about?

At this time I am working with several collaborators on the interaction between metabolism and the immune system. Emerging research demonstrates connections between the immune system and metabolism, both mitochondrial disorders and oxidative stress. We have recently published a review article on mitochondrial dysfunction in autism which discussed this (https://www.ncbi.nlm.nih.gov/pubmed/30039193) and previously Dr Rossignol and I published a review article outlining the evidence for connection between these abnormalities in the brain of children with ASD (https://www.ncbi.nlm.nih.gov/pubmed/24795645). I think this is a promising area of research which may pave the way for new treatment targets.

You’ve published “Autism Spectrum Disorder in The Emergency Department: Looking Beyond Behavior.” What should ER physicians, primary care providers, and specialists be considering when a patient with autism presents with acute behavioral or neuropsychiatric symptoms?

It is very important to consider that there may be medical issues that can be driving behavioral decompensation. These medical abnormalities do not have to be complicated immune and/or metabolic abnormalities but may be more basic problems such as sleep disruption, gastrointestinal disorders and/or anxiety which may need to be evaluated and addressed. There may also be other underlying more complicated metabolic and/or immune disorders, so it is important to consider referring the child to a practitioner experienced in looking into these treatable abnormalities. Most importantly, it is important to have a vision of try to treat the underlying biological cause of the symptoms rather than just treating the behavior with medications to suppress it. Indeed, disruptive behavior may be signaling that something that is not obvious needs to be addressed and suppressing this signal may simple make a untreated medical problem worse by allowing it continue and progress without appropriate treatment.

-The Foundation For Children With Neuroimmune Disorders thanks Dr. Richard Frye for taking the time to allow FCND Founder and President Anna Conkey to interview him.

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I Know You’re In There: Restoring Balance preview

Sometimes our struggles shape who we are! But don’t you wish we didn’t have to struggle so much with our children who are on the spectrum? This is a 90 second clip of Ryan Hinds who is recovered from autism. Ryan’s parents were told there was no recovery from autism. There was no cure. There was no hope. The “experts” said Ryan should be institutionalized. But they were wrong. Ryan’s recovery was not miraculous. It was the result of having his medical illness treated. Ryan now works as an aerospace engineer. And what his parents wanted most for their son actually happened…he is happy, has friends, and leads a typical life. You can preview Ryan’s recovery story called I KNOW YOU’RE IN THERE on Amazon or at http://a.co/a7PiCyQ

MEDICAL SCIENCE proceeds along a hierarchy of evidence; often, patients are studied individually (case studies), or a small collection of patients are examined and characterized together (case series studies). Case series studies typically have smallish sample sizes and it is generally understood that larger studies will be necessary to determine more accurately the characteristics being studied.

In a new case series study, brain tissue from 14 donors with a diagnosis of MS was studied in a case series by Mold et al (2018) using transversely heated graphite furnace atomic absorption spectrometry. The study found high aluminum content (>10 ug/g dry weight) in all areas of the brain studied, with some areas exceeding 50 ug/g. They found aluminum both with cells and in the interstitium between cells. They found aluminum co-localised with structures known to be present in Secondary Progressive Multiple Sclerosis (SPMS) in the frontal cortex of one donor with SPMS.

There are a number of critical lines of evidence that make this fundamental finding critically important. Patients with MS have lower amounts of aluminum in their hair, suggesting depressed detoxification, and higher amounts are found in urine on chelation challenge testing (Fulgenzi et al., 2014). Chelation with EDTA is known to significantly reduce aluminum intoxication (Fulgenzi et al. 2014), and consumption of silica-rich mineral waters also increase urinary excretion of aluminum from patients with SPMS (Jones et al., 2017).

Extremely plausible direct mechanisms of the cause of MS from aluminum are known and animal studies routinely induced MS using aluminum hydroxide injections. So much evidence exists that points to aluminum as a source of strange new conditions of unknown causes, such as MMF and Gulf War Syndrome, one would think that calls to reconsider the use of aluminum in vaccines would be answered. The same team had previously found high amounts of aluminum in the brains of people with autism, and and in patients with Alzheimer’s disease. The latter result, while also important, is not surprising, as it has long been known that amyloid is part protein and part aluminum. Finally, when France brought on HepB vaccination, cases of MS following vaccination increased; when they stopped recommending the HepB vaccine, which contains aluminum hydroxide, the rate of HepB vaccine-associated MS cases dropped to near zero.

Complicity

What is surprising is the lack of action on the part of the US FDA to put an end to the use of this dangerous metal in vaccines, and that the NIH is not funding more studies like this. NIH should fund studies to determine how to most safely remove aluminum from anyone exposed via vaccines; brain stem amyloidosis is a non-trivial concern. Approaches like ketogenic diet, silica-rich mineral waters, hyperbaric oxygen, EDTA, intranasal insulin and intranasal deferoxamine (to prevent brain stem amyloidosis) should all be tested in randomized clinical trails in clinical populations known to be afflicted with aluminum intoxication (autism, Alzheimer’s, MS).

What is also surprising is that the CDC and ACIP remain blithe to the morbidity and mortality their continued approval of vaccines that contain metals like aluminum and mercury. They make decisions on behalf of us all, and yet every member of ACIP with the exception of one military member has conflicts of interest with vaccine manufacturers. ACIP should review all of the literature on aluminum and make recommendations on how to phase it, and thimerosal, out of vaccines completely.

Further inaction on the part of these regulatory and funding agencies, and active denialism at this point will surely be seen by future generations as both callous disregard, and where conflicts of interest reside, complicity.

The study, conducted at the Keele University, was funded in part by the Children’s Medical Safety Research Institute.

Lyme disease can cause delayed neurologic symptoms similar to those seen in multiple sclerosis (MS) such as weakness, blurred vision caused by optic neuritis, dysesthesias (sensations of itching, burning, stabbing pain, or “pins and needles”), confusion and cognitive dysfunction, and fatigue. Lyme disease symptoms may also have a relapsing-remitting course. In addition, Lyme disease occasionally produces other abnormalities that are similar to those seen in MS, including positive findings on magnetic resonance imaging (MRI) scans of the brain and analysis of cerebrospinal fluid (CSF).

These similarities in symptoms and test results have led some people with MS to seek testing for the presence of antibodies to Borrelia, to determine if their neurologic symptoms are the result of Lyme disease or truly MS. The distinction is important because Lyme disease, especially when treated early, often responds to antibiotic therapy, whereas MS does not.

Studies examining Lyme disease & MSTwo studies have examined the overlap in diagnosis of MS and Lyme disease. The studies were conducted in parts of Long Island, New York, an area where Lyme disease is endemic, or regularly found.

In the first study, people who had Borrelia antibodies in their blood as well as a variety of neurologic symptoms considered to be “MS-like,” were evaluated with MRI, evoked potentials (EP) and CSF analysis, including a test for the presence of Borrelia antibodies in the spinal fluid.

While those with the MS-like illness had the highest incidence of abnormal MRIs and were the only ones among those studied to have abnormal EP and oligoclonal bands in their spinal fluid (indicating an abnormal immune response), they did not prove to have any Borrelia antibody in their spinal fluid.

The researchers concluded that the few patients with the MS-like symptoms probably had these symptoms due to MS and had also been exposed to the Borrelia bacterium.A companion study looked for the presence of Borrelia antibodies in the blood of 100 people with the diagnosis of possible MS. Of 89 people who in fact turned out to have definite MS, only one had Borrelia antibodies. The researcher concluded that “…infection with Borrelia is infrequent in MS patients who live in an endemic area. Lyme disease is unlikely to be a significant factor in the differential diagnosis of MS.” Furthermore, the presence or antibodies to Borrelia does not prove that Borrelia is causing the neurological symptoms, only that there has been previous infection with the organism.

Just remember, “rare” is only “rare” if it isn’t you.

I repost the following article because Lyme/MSIDS patients have chronically high inflammation within the body and many struggle with MCAS as well. Please read the following article and consider your own symptoms. Discuss these with your doctor.

Mast Cell Disease and Vaccination: Is There Increased Risk?

Do you or does someone you know have severe symptoms of itching, rashes, flushing, stomach or other body pain, frequent diarrhea, nausea, fatigue, brain fog, headache and severe allergies to certain foods, medications or insect stings that may include fainting episodes or anaphylaxis? Although it has been classified as a rare immune system disorder, there are indications that Mast Cell Activation Syndrome (MCAS) may be more prevalent than previously thought and people can suffer for years without being correctly diagnosed.1With severe allergies and chronic inflammatory diseases increasing in populations around the world, scientists are investigating the association between mast cell dysregulation and various brain and immune system disorders ranging from asthma, inflammatory bowel disease and chronic fatigue syndrome to ADHD, depression, autism and cancer.2345

What are Mast Cells?

Mast cells are often described as the body’s sentinels because they modulate and orchestrate the immune response and play a critical role in innate and adaptive immunity, as well as maintaining homeostasis in the body.67 Mast cells and basophils are types of white blood cells (granulocytes) that are made in the bone marrow. While basophils circulate in the blood, mast cells reside in tissues, primarily connective and mucosal tissues near blood vessels and nerves of the skin, gastrointestinal, respiratory and genitourinary tracts, and the brain.8 9

Mast cells and basophils are part of the body’s first line of defense when responding to injury or foreign antigens, such as pathogenic bacteria, viruses, parasites, protozoa, fungi and toxins.10 During the immune system’s normal protective response to a perceived threat, mast cells can release over 200 potent pro-inflammatory mediators within seconds of activation, including histamine (amino acid product), heparin (anti-coagulant), tryptase (enzyme) and cytokines (cell signaling protein molecules).1112

The activation of this normal protective inflammatory response to internal or external stress increases blood flow to the site of the infection or wound to aid in healing. Acute inflammatory responses are often accompanied by the four classic signs of redness, heat, swelling and pain, which eventually disappear as cells regenerate and inflammation resolves during the healing process.13 However, allergic inflammatory responses are also provoked by mast cell activation.14

What is Mast Cell Disease and MCAS?

Mast cell activation is common and helps combat threats to our health. However, when a dysregulated immune system overproduces mast cells or when mast cell activation is out of proportion to the perceived internal or external threat, it can compromise our health.

The most serious of mast cell activation diseases (MCAD) is systemic mastocytosis, which can develop when genetically altered mast cells infiltrate and accumulate in large numbers in major organ systems, such as the skin, liver and intestines.1516 A rare form of MCAD is aggressive systemic mastocytosis, usually caused by somatic mutations in the KIT gene, which progresses rapidly and causes organ damage and failure.17 An even rarer form of mast cell disease is mast cell leukemia and mast cell sarcoma.18

Mast Cell Activation Syndrome (MCAS) is a common variation of mast cell disease and can be more or less severe depending upon epigenetic, environmental, lifestyle and other host factors. MCAS occurs when a normal amount of mast cells inappropriately and chronically release histamine and other pro-inflammatory mediators that can lead to persistent inflammation in one or more parts of the body. Over time, chronic inflammation can damage cells if inflammation cannot be resolved and every organ in the body can be affected.19

Systemic mastocytosis is estimated to affect 1 in 10,000 people. However, the prevalence of MCAS is not known and some researchers estimate the less serious forms of mast cell dysregulation could affect between 10 and 30 percent of populations.2021

Symptoms of MCAS

Symptoms of MCAS can wax and wane and often various symptoms start in early childhood, although people generally do not get diagnosed for decades after symptoms appear. The effects of mast cell dysregulation can cause a plethora of diverse symptoms, depending on where the mast cells are activated in the body.

When mast cells overeact to a benign substance as if it were a foreign antigen posing a serious threat, symptoms can be life threatening like when a person has an anaphylactic reaction to peanuts.24 Mast cell over-activation and release of large amounts of histamine in the body can be unpredictable, so people with MCAS are at risk of reacting to different foods, alcohol or medications at any time, leaving them uncertain as to when they might have another reaction to something they previously were not aware was a trigger for mast cell activation.25Many people with MCAS carry an epi-pen with them in case of anaphylaxis.

Diagnosing mast cell disease is difficult and involves blood and urine testing and, less frequently, skin or bone marrow biopsy.26 Most medical doctors in general practice are not well informed about MCAS, while doctors specializing in functional medicine tend to be more familiar with symptoms. Functional medicine focuses on a personalized, integrative approach to investigating root causes of health problems by analyzing the unique genetic, epigenetic, biochemical, environmental and lifestyle factors that affect an individual’s immune function and influence the development of complex chronic diseases.

Because MCAS can present differently in different people, the goal is to identify individual triggers for mast cell activation, including food (such as gluten, dairy, baker’s yeast, shellfish, nuts, wheat, corn); or chemicals (alcohol, certain prescription medications, MSG, aspartame, artificial dyes, cleaning products); mold and spores; extreme heat or cold; vigorous exercise; stress or other potential triggers and avoid them.27 There are many unanswered questions about mast cell disease and few prescription drug treatments.28 There is evidence that certain flavonoids (such as Quercetin and Rutin) inhibit histamine release and expression of pro-inflammatory cytokines in mast cells.29

MCAS and Chronic Disease

Because overactive mast cells release pro-inflammatory mediators causing widespread inflammation in the body, MCAS has been implicated in a number of diseases that involve chronic inflammation and immune dysfunction. There is evidence that MCAS is related to allergic/inflammatory diseases, autoimmune disorders, and autism spectrum disorder.3031

Symptoms of Histamine Intolerance

Histamine is a neurotransmitter that facilitates communications between neurons throughout the nervous system. Histamine levels in the body help control the sleep and wake cycle and influence metabolism, thyroid function, reproduction and management of stress, as well as regulate body temperature, maintain fluid balance in the body and other important functions. Histamine can also increase permeability of the blood brain barrier.35

People with histamine intolerance lack sufficient levels of Diame oxidase (DAO), a gut enxyme, and histamine N-methyltransferase (HNMT), a liver enzyme, which break down and detoxify histamine in foods, medications or alcohol. When these enzymes fail to do their job, high levels of histamine circulate in the blood and cause histamine intoxication.36 Eating histamine-rich foods, drinking alcohol or taking prescription drugs that release histamine and or inhibit DAO or HNMT enzyme activity can cause high histamine levels and symptoms like diarrhea, headache, sinus congestion, heart palpitations, itching and flushing, low blood pressure and many other symptoms.

The symptoms of histamine intolerance and MCAS are similar and a person can have either histamine intolerance of MCAS or both. The main difference between the two is that histamine intolerance involves the triggering of high levels of histamine in the blood that cannot be efficiently detoxified, while MCAS involves dysregulated mast cells releasing not only histamine but multiple inflammatory and other types of mediators in tissues of the body.37

There is some evidence for genetic predisposition to histamine intolerance. Like MCAS, histamine intolerance can be hard to diagnose even with blood and urine tests. Treatment for histamine intolerance focuses on avoiding histamine rich foods and alcohol or medications that block DAO or HNMT enzyme activity. Some people with histamine intolerance take DAO supplements to help the body break down histamine or take anti-histamines to control levels of histamine in the blood.38

MCAS and Autism Spectrum Disorder

Over the past decade, a number of reports and studies have linked Autism Spectrum Disorder (ASD) with immune dysregulation and chronic inflammation in the body, including in the brain.394041 There is evidence that mast cell dysregulation is associated with Autism Spectrum Disorder (ASD).4243

Some researchers have suggested that the relationship between immune response and brain function may be negatively affected when toxins cross the blood brain barrier during a critical point in neural development, causing neurotoxicity and immune dysregulation that disrupts the natural neuron pruning process and contributes to the development of autism spectrum disorders. 44 If the immune system is dysregulated, it can affect the formation and necessary removal of physical connections between neurons that is critical to maintaining healthy brain cell function.45

ASD children have a higher rate of allergies (30%) compared to neurotypical children (2.5%). Tufts University Professor Theodore Theoharides, PhD, MD, who has conducted extensive research into mast cell disorders, has published a series of studies on the association between MCAS and autism. The evidence he has provided suggests that overactive mast cells in the brain and gut triggered by non-allergic stimulus can lead to brain inflammation and chronic brain dysfunction with symptoms diagnosed as autism. Evidence that mast cells play a role in ASD is also supported by the fact that the hypothalamus, which regulates behavior and language, houses the majority of mast cells in the brain and people with ASD often have problems associated with language and behavior.46

What Are Co-Factors for Developing MCAS?

Currently, MCAS is not considered to be a genetically inherited disease but there is evidence for epigenetic predisposition to development of MCAS as it tends to run in families, albeit with varying degrees of severity and presentations in individuals within the same family.47 Perinatal stress, environmental exposures, DNA methylation, somatic genetic mutations and interactions between microbiota and mast cells have been proposed as contributing co-factors.484950

According to University of Minnesota Professor Lawrence Afrin, MD, an oncologist and leading mast cell authority, mast cell disease can present with different manifestations and outcomes for each person because every person is unique:

“Conveying a new understanding that all mast cell disease features inappropriate mast cell activation, the new top level mast cell activation disease (MCAD) encompasses various types of rare mastocytosis and likely prevalent mast cell activation syndrome (MCAS). The apparent uniqueness in each patient with MCAD of constitutively activating mutational patterns in KIT and other mast cell regulatory elements likely is the principal driver of not only the specific clinical presentation, and therapeutic response profile, in each patient but also the great heterogeneity across this population.”51

Inflammation and Vaccination

When the immune system repeatedly mounts an inappropriate acute inflammatory response to antigens or non-allergic substances, it can lead to unwanted chronic inflammation in the body that is common to a number of immune and neuroimmune system disorders.5253Vaccination stimulates an inflammatory immune response that promotes production of antibodies and the acquisition of artificial active immunity.54 However, unlike naturally acquired immunity that involves a normal inflammatory response producing both innate (cellular) and humoral (adaptive) immunity, most vaccines manipulate the immune system in way that only stimulates production of vaccine strain antibodies and humoral immunity.55

Because vaccine acquired artificial immunity is temporary, many vaccines contain adjuvants, such as aluminum or squalene, to stimulate a strong inflammatory response in the body, which involves mast cell activation.56 There is mounting scientific evidence that when individuals cannot tolerate hyper-stimulation of the immune system, the atypical inflammatory response to vaccination can remain unresolved, become chronic, and lead to allergy and autoimmunity.57

Vaccines contain many ingredients, including chemicals, virus like protein particles and heavy metals, such as aluminum adjuvants and mercury (Thimerosal) preservatives, as well as other substances that can cause inflammation.5859 Mercury can activate and destabilize mast cells,6061 which disrupts the blood brain barrier and makes it easier for mercury to enter the brain where it can remain for long periods of time.62 Even a low concentration of mercury has been shown to activate mast cell mediators in the brain. Scientists have demonstrated that Thimerosal-derived ethylmercury is a mitochondrial toxin and may damage mitochondrial DNA.63

Polysorbate 80 is a chemical emulsifier added to some vaccines. Polysorbate 80 has the ability to help deliver substances across the protective blood brain barrier and into the brain.64When toxins enter the brain, mast cells are activated and cause inflammation.65 Polysorbate 80 has also been shown to increase histamine levels in animal studies.66

The first vaccine found to cause acute and chronic brain inflammation (acute and chronic encephalopathy) and permanent brain dysfunction was smallpox vaccine created by Edward Jenner in 1796.67 The first vaccine found to cause acute and chronic encephalopathy with permanent brain dysfunction that ranged from learning disabilities and behavior disorders to profound mental retardation was whole cell pertussis vaccine licensed in 1915 and combined in 1949 with diphtheria and tetanus vaccine to create DPT vaccine.6869 Whole cell pertussis vaccine ingredients include pertussis toxin, endotoxin, aluminum and mercury.70

Cases of pertussis vaccine-related brain inflammation followed by development of autism were first described in the book DPT: A Shot in the Dark published in 1985.7172

Is Mast Cell Disease a Risk Factor for Vaccine Reactions?

Mast cells play an important part in keeping the body healthy, but when they malfunction, can cause system wide chronic inflammation in the body that interferes with quality of life or can even cause death.

Dr. Afrin recently related the story of a patient,

“who in the first year of his life had been perfectly normal and then, within hours of his first DTP vaccine at age one, developed into just a terrible multi-system inflammatory mess, including essentially acute onset autism.” When he was 20 years old, biopsies tested positive for mast cells. He was subsequently treated for MCAS with remarkable improvement.73

Most babies in the U.S. are being given 25 doses of nine different vaccines (or more) by their first birthday and can receive eight or more vaccines simultaneously.74 As mentioned previously, there are ingredients in vaccines that provoke inflammatory responses in the body that involve mast cell activation.75

Although for the past several decades, most pediatricians and public health officials have rejected the possibility of a relationship between vaccination and the development of allergic and autoimmune disorders,76 the apparent increase in mast cell dysregulation in highly vaccinated populations deserves more in-depth investigation.

The two outstanding questions are:

Does repeated atypical manipulation of the immune system with multiple vaccines in early life trigger MCAS or development of histamine intolerance in genetically or epigenetically predisposed individuals?

Are individuals with undiagnosed MCAS or histamine intolerance at greater risk for suffering vaccine reactions, particularly if they have a personal or family history of allergy or autoimmunity?

There is urgent need for more basic science research into how and why MCAS and histamine intolerance occurs and whether vaccination is a co-factor in increasing individual risks for mast cell dysregulation.